Hosts:

• Pradip Kamat, Children’s Healthcare of Atlanta/Emory University School of Medicine
• Rahul Damania, Cleveland Clinic Children’s Hospital

Introduction

Today, we discuss the case of an 8-month-old infant with severe bronchospasm and abnormal blood gas. We'll delve into the epidemiology, pathophysiology, and evidence-based management of acute bronchiolitis.

Case Summary

An 8-month-old infant presented to the ER with decreased alertness following worsening work of breathing, preceded by URI symptoms. The infant was intubated and transferred to the PICU, testing positive for RSV. Initial blood gas showed 6.8/125/-4, and CXR revealed massive hyperinflation. Vitals: HR 180, BP 75/45, SPO2 92% on 100% FIO2, RR 12 (prior to intubation), now around 16 on the ventilator, afebrile.

Discussion Points

• Etiology & Pathogenesis: Bronchiolitis is primarily caused by RSV, with other viruses and bacteria playing a role. RSV bronchiolitis is the most common cause of hospitalization in infants, particularly in winter months. Immuno-pathology involves an unbalanced immune response and can lead to various extra-pulmonary manifestations.
• Diagnosis: Diagnosis is clinical, based on history and examination. Key signs include upper respiratory symptoms followed by lower respiratory distress. Blood gas, chest radiography, and viral testing are generally not recommended unless warranted by severe symptoms or clinical deterioration.
• Management Framework: For patients requiring PICU admission, focus on oxygenation and hydration. High-flow therapy and nasal continuous positive airway pressure (CPAP) can be used. Hydration and feeding support are crucial. Antibiotics, steroids, and bronchodilators are generally not recommended. Mechanical ventilation and ECMO may be necessary in severe cases.
• Immunoprophylaxis & Nosocomial Infection Prevention: Palivizumab and nirsevimab are used for RSV prevention in high-risk infants. Strict infection control measures, including hand hygiene and isolation, are essential to prevent nosocomial infections.

Conclusion

RSV bronchiolitis is a common and potentially severe respiratory illness in infants. Management focuses on supportive care, with a careful balance between oxygenation and hydration. Immunoprophylaxis and infection control are crucial in preventing the spread of the virus.

Thank you for listening to our episode on acute bronchiolitis. Please subscribe, share your feedback, and visit our website at picudoconcall.org for more resources. Stay tuned for our next episode!

References

Rogers - Textbook of Pediatric Critical Care Chapter 49: Pneumonia and Bronchiolitis. De Carvalho et al. page 797-823

Reference 1: Dalziel, Stuart R; Haskell, Libby; O'Brien, Sharon; Borland, Meredith L; Plint, Amy C; Babl, Franz E; Oakley, Ed. Bronchiolitis. The Lancet. , 2022, Vol.400(10349), p.392-406. DOI: 10.1016/S0140-6736(22)01016-9; PMID: 35785792

Reference 2: Schroeder AR, Destino LA, Ip W, Vukin E, Brooks R, Stoddard G, Coon ER. Day of Illness and Outcomes in Bronchiolitis Hospitalizations. Pediatrics. 2020 Nov;146(5):e20201537. doi: 10.1542/peds.2020-1537. PMID: 33093138.

Hosts:

• Pradip Kamat, Children’s Healthcare of Atlanta/Emory University School of Medicine
• Rahul Damania, Cleveland Clinic Children’s Hospital

Case Introduction:

• 6-year-old patient admitted to PICU with severe pneumonia complicated by pediatric Acute Respiratory Distress Syndrome (pARDS).
• Presented with respiratory distress, hypoxemia, and significant respiratory acidosis.
• Required intubation and mechanical ventilation.
• Despite initial interventions, condition remained precarious with persistent hypercapnia.

Physiology Concept: Dead Space

• Defined as the volume of air that does not participate in gas exchange.
• Consists of anatomic dead space (large airways) and physiologic dead space (alveoli).
• Physiologic dead space reflects ventilation-perfusion mismatch.

Pathological Dead Space:

• Occurs due to conditions disrupting pulmonary blood flow or ventilation.
• Common in conditions like pulmonary embolism, severe pneumonia, or ARDS.

Clinical Implications:

• Increased dead space fraction (DSF) in PARDS is a prognostic factor linked to severity and mortality.
• Elevated DSF indicates worse lung injury and inefficient gas exchange.
• DSF can be calculated using the formula: DSF = (PaCO2 – PetCO2) / PaCO2.

Practical Management:

• Optimize Mechanical Ventilation
• Enhance Perfusion
• Consider Positioning (e.g., prone positioning)

Summary of Physiology Concepts:

• Bohr equation for physiologic dead space.
• Importance of lung-protective ventilation strategies.
• Monitoring and trending dead space fraction.
• Strategies to improve airway patency and mucociliary clearance.

Connect with us!

• PICU Doc on Call provides concise explanations of critical concepts in pediatric intensive care.
• Feedback, subscriptions, and reviews are encouraged.
• Visit picudoconcall.org for episodes and Doc on Call infographics.
• Hosted by Dr. Pradip Kamat and Dr. Rahul Damania.

Reference:

• Yehya N, Bhalla AK, Thomas NJ, Khemani RG. Alveolar Dead Space Fraction Discriminates Mortality in Pediatric Acute Respiratory Distress Syndrome. Pediatr Crit Care Med. 2016 Feb;17(2):101-9. doi: 10.1097/PCC.0000000000000613. PMID: 26669646; PMCID: PMC4740261.

Today's episode promises an insightful exploration into a unique case centered on retropharyngeal abscess in the PICU, offering a comprehensive analysis of its clinical manifestations, pathophysiology, diagnostic strategies, and evidence-based management approaches.

Today, we unravel the layers of a compelling case involving a 9-month-old with a retropharyngeal abscess, delving into the intricacies of its diagnosis, management, and the critical role played by PICU specialists. Join us as we navigate through the clinical landscape of RPA, providing not only a detailed analysis of the presented case but also valuable takeaways for professionals in the field and those aspiring to enter the world of pediatric intensive care. Welcome to PICU Doc On Call – where MED-ED meets the real challenges of the PICU.

• Patient: 9-month-old male with rapid symptom onset, left neck swelling, fever, noisy breathing, and decreased oral intake.
• Initial presentation: Left neck swelling, limited neck mobility, and deteriorating condition.
• Imaging: Neck X-ray and CT scan with IV contrast confirmed Retropharyngeal Abscess (RPA).
• Management: High-flow nasal cannula, intravenous antibiotics, and consultation with ENT. PICU admission for comprehensive care.

• Rapid Symptom Onset
• Neck Swelling & Drooling
• Limited Neck Mobility

• A previously healthy 9-month-old male with a recent upper respiratory infection, presenting with rapid-onset left neck swelling, fever, and respiratory distress. Imaging suggestive of a Retropharyngeal Abscess, requiring urgent PICU management for airway protection and antibiotic therapy.

• Anatomy of retropharyngeal space
• Rapid communication of infections via lymph nodes
• Infection sources: dental issues, trauma, localized infections (e.g., otitis, URI)

• Airway compromise and posterior mediastinitis
• Progression from cellulitis to abscess
• Microbial suspects: Group A Streptococcus, anaerobes, Staphylococcus aureus, Haemophilus influenza, Klebsiella, Mycobacterium avium-intracellulare

• Seen predominantly in children aged 3-4 years
• Non-specific symptoms in the acute setting
• Pronounced symptoms in PICU: neck pain, stiffness, torticollis, muffled voice, stridor, respiratory distress

• Thorough history and physical examination
• CT scan with contrast as the gold standard
• Blood culture, CRP, and procalcitonin for infection severity

• Limited neck mobility is the most specific physical exam finding
• Younger age and signs of airway obstruction indicate a complicated course

• Antibiotic therapy: Up to 50% cases can be treated with IV antibiotics
• Surgical drainage may be needed if no improvement or persistent respiratory distress
• Duration of therapy: 10 to 14 days
• Controversial use of steroids for reducing airway swelling

• Upper airway obstruction, aspiration pneumonia, internal jugular thrombosis, carotid artery sheath rupture
• Mediastinitis: severe inflammation, infection of mediastinal tissues

• Respiratory viral panel: RSV, adenovirus, rhino/enterovirus
• Intubation due to worsening respiratory distress
• Incision and drainage (I&D) by ENT
• Cultures grew MRSA
• Extubation after air leak detection; discharged on oral Clindamycin

• Maintain a low threshold for suspecting RPA
• Initiate broad-spectrum antibiotics early
• Prioritize airway assessment and intervene early in cases of worsening upper airway obstruction or hypoxia
• Consider surgical drainage for non-responders, escalating respiratory distress, or immunocompromised patients

• Emphasize the critical nature of RPA in children and the importance of early intervention.
• Complications include upper airway obstruction, aspiration pneumonia, and potential vascular complications.

• Villanueva-Fernández E, et al. (2022) Role of steroids in conservative treatment of parapharyngeal and retropharyngeal abscess in children. Eur Arch Otorhinolaryngol.
• Akhavan M. (2021) Ear, Nose, Throat: Beyond Pharyngitis: Retropharyngeal Abscess, Peritonsillar Abscess, Epiglottitis, Bacterial Tracheitis, and Postoperative Tonsillectomy. Emerg Med Clin North Am.
• Reilly BK, Reilly JS. (2012) Retropharyngeal abscess: diagnosis and treatment update. Infect Disord Drug Targets.

Today, Dr. Pradip Kamat (Children’s Healthcare of Atlanta/Emory University School of Medicine) and Dr. Rahul Damania (Cleveland Clinic Children’s Hospital), are excited to speak with Matthew Kirschen, MD, PhD, FAAN, FNCS, regarding a very sensitive topic involving pediatric brain death guidelines published in 'Neurology' in October 2023. Dr. Matthew Kirschen, a leader in pediatric neurocritical care and one of the authors of the new guidelines.

Guest Introduction:

Dr. Matthew Kirschen is an Assistant Professor of Anesthesiology and Critical Care Medicine, Pediatrics, and Neurology at the Children's Hospital of Philadelphia. A proud alumnus of Brandeis University and Stanford, where he secured both his MD and PhD in neuroscience. Dr. Kirschen’s journey includes a residency at Stanford followed by a unique dual fellowship in neurology and pediatric critical care at CHOP. Notably, he's among the rare professionals dual-boarded in both PCCM and Neurology.

Dr. Kirschen’s tireless endeavors in pediatric neuro-critical care, especially his work on multimodal neuro-monitoring to detect and prevent brain injuries in critically ill children, have garnered significant attention. His expertise also extends to predicting recovery post-severe brain injuries. Pertinent to today's discussion, Dr. Kirschen has displayed a keen interest in the precise diagnosis of brain death and proudly stands as one of the authors of the new guidelines on the topic of Pediatric and Adult Brain death/death by neurologic criteria.

Discussion:

1. Understanding Brain Death Criteria:

• Brain Death/Death by Neurologic Criteria (BD/DNC) declared with permanent cessation of all brain functions, including brainstem
• Important considerations before BD/DNC determination:
• No evaluation in infants < 37 weeks corrected gestational age
• Absence of coma, intact brainstem reflexes, and spontaneous breathing inconsistent with BD/DNC

2. Who Can Perform BD/DNC Evaluations:

• Attending clinicians must be credentialed and trained in BD/DNC evaluation.
• Two attending clinicians are needed for evaluation, with exceptions for advanced practice providers.

3. Prerequisites for BD/DNC Determination:

• Importance of identifying the etiology of BD/DNC to avoid reversible processes
• Observation periods based on age and type of brain injury
• Maintaining core body temperature before evaluation

4. Blood Pressure Management:

• Hypotension can lead to impermanent coma; clinicians should manage with fluids or vasopressors.
• Specific blood pressure targets for different ECMO support types

5. Medication Considerations:

• Excluding medications affecting CNS function before BD/DNC evaluation
• Recommendations for drug level monitoring and metabolic derangement exclusion

6. Performing the BD/DNC Neurologic Examination:

• Two independent examinations by different clinicians with a minimum 12-hour interval
• Central components including assessing irreversible coma and brainstem reflexes

7. Apnea Testing:

• Two apnea tests after each neurologic examination
• Procedures, complications, and baseline PCO2 and pH considerations

8. Ancillary Tests:

• BD/DNC remains a clinical evaluation; ancillary tests are used in specific circumstances.
• Conditions and circumstances for using or not using ancillary tests

9. Case Presentation and Family Communication:

• Real-life case presented and discussed following the new AAN guidelines.
• No need for consent before evaluation; communication with the family emphasized.
• Maintaining transparency and involvement in the BD/DNC process

10. Public Trust in BD/DNC:

• Building trust through education, transparency, public involvement, and ethical considerations
• Continuous improvement, professional collaboration, and legal frameworks

We welcome you to share your feedback, subscribe & place a review on our podcast! Please visit our website picudoconcall.org which showcases our episodes as well as our Doc on Call management cards. PICU Doc on Call is co-hosted by Dr. Pradip Kamat and Dr. Rahul Damania. Stay tuned for our next episode! Thank you!

References:

• Greer D, Kirschen MP et al. Pediatric and Adult Brain Death/Death by Neurologic Criteria Consensus Guideline Report of the AAN Guidelines Subcommittee, AAP, CNS, and SCCM. Neurology 2023; 101:1-21. doi:10.1212/WNL.0000000000207740
• Pediatric Neurocritical Care Educational Series - Lecture_ Brain Death 2023 Guidelines

Today’s case presentation involves a 2-year-old girl who was previously healthy and was admitted to the Pediatric Intensive Care Unit (PICU) for acute respiratory distress characterized by increased work of breathing and wheezing.

A 2-year-old girl with acute respiratory distress due to RSV infection

• Presented with increased work of breathing, wheezing, and no fever
• Started on High Flow Nasal Cannula (HFNC) therapy in the PICU

Key Elements:

• Prodrome of URI symptoms
• Increased respiratory effort (nasal flaring, intercostal retractions, decreased lung base air entry)
• HFNC improved the work of breathing and oxygen saturation

Washout of Nasopharyngeal Dead Space:

• HFNC clears nasopharyngeal dead space, improving oxygen efficiency.
• Reduces re-breathing of CO2 from the anatomical dead space.
• Enhances ventilation efficiency and oxygenation.

Reduction in Upper Airway Resistance:

• HFNC reduces resistance in the upper airway.
• Delivers rapid gas flow matching or exceeding natural inhalation rate.
• Eases breathing, especially in neonates and infants with narrow airways.

Optimal Conditioning of Gas:

• HFNC delivers heated and humidified oxygen, matching the body's conditions.
• Reduces energy expenditure and risk of airway irritation
• More comfortable and effective compared to cold, dry air delivery

• HFNC generates minimal and variable PEEP.
• Amount of PEEP depends on factors like flow rate and cannula size
• Not as high or consistent as other respiratory support devices

• A 2022 CHEST study by Khemani et al. on children with bronchiolitis challenged the conventional understanding of HFNC's mechanisms.
• HFNC primarily reduces breathing effort but does not consistently increase lung volume (EELV) or tidal volume (VT).
• Reduction in the pressure rate product (PRP) indicates decreased breathing effort, but not significant alterations in EELV or VT.

• HR, RR, and SpO2 are key indicators of HFNC efficacy.
• HR and RR should approach normal ranges for the child's age.
• Improvement in SpO2 levels while maintaining or reducing FiO2 indicates a positive response.

• HFNC is a valuable tool in pediatric care for alleviating respiratory distress.
• Not a one-size-fits-all solution; vigilant monitoring and reassessment are crucial
• Recognizing HFNC's mechanisms allows for optimized bedside application.

Closing Remarks:

• Subscribe, share feedback, and leave a review on the podcast.
• Visit picudoconcall.org for more episodes and management cards.
• Hosted by Dr. Pradip Kamat and Dr. Rahul Damania

Miller AG, Gentle MA, Tyler LM, Napolitano N. High-Flow Nasal Cannula in Pediatric Patients: A Survey of Clinical Practice. Respir Care 2018; 63:894.

Wraight TI, Ganu SS. High-flow nasal cannula use in a pediatric intensive care unit over 3 years. Crit Care Resusc 2015; 17:197.

Hutchings FA, Hilliard TN, Davis PJ. Heated humidified high-flow nasal cannula therapy in children. Arch Dis Child 2015; 100:571.

Lee JH, Rehder KJ, Williford L, et al. Use of high flow nasal cannula in critically ill infants, children, and adults: a critical review of the literature. Intensive Care Med 2013; 39:247.

Wing R, James C, Maranda LS, Armsby CC. Use of high-flow nasal cannula support in the emergency department reduces the need for intubation in pediatric acute respiratory insufficiency. Pediatr Emerg Care 2012; 28:1117.

Bressan S, Balzani M, Krauss B, et al. High-flow nasal cannula oxygen for bronchiolitis in a pediatric ward: a pilot study. Eur J Pediatr 2013; 172:1649.

Mayfield S, Bogossian F, O'Malley L, Schibler A. High-flow nasal cannula oxygen therapy for infants with bronchiolitis: pilot study. J Paediatr Child Health 2014; 50:373.

Kelly GS, Simon HK, Sturm JJ. High-flow nasal cannula use in children with respiratory distress in the emergency department: predicting the need for subsequent intubation. Pediatr Emerg Care 2013; 29:888.

Welcome to PICU Doc on Call, a podcast dedicated to current and aspiring intensivists. I'm Pradeep Kumar coming to you from Children's Healthcare of Atlanta, Emory University School of Medicine, and I'm Rahul Damania from Cleveland Clinic Children's Hospital. We are two pediatric ICU physicians passionate about all things medical education in the PICU.

Episode Overview: 

PICU.com call focuses on interesting PICU cases and management in the acute care Pediatric setting. In this episode, we discuss the case of an eight-year-old boy with chest pain, fatigue, and shortness of breath. This case presentation by Rahul highlights the complexity of pediatric care in the PICU.

Case Presentation: 

An eight-year-old boy with up-to-date immunizations and no recent travel or pet exposure presented to the PICU with chief complaints of chest pain, fatigue, and decreased oral intake. His history over the preceding two weeks included a diminishing appetite, episodes of vomiting, and shortness of breath.

On examination, he exhibited various cardiac findings, including a hyperdynamic left ventricle, murmurs, and a noted gallop. Abdominal and neurological findings were also concerning. Diagnostic studies revealed an enlarged heart, and sinus tachycardia with left ventricular hypertrophy, and echocardiography confirmed severe valvular and ventricular abnormalities.

Laboratory Findings:

Laboratory findings included elevated BNP, slightly elevated troponin, and elevated inflammatory markers (ESR and CRP). Strep throat culture was negative, but ASO and anti-DNAse B titers were markedly elevated. MRI confirmed multiple punctate infarctions, likely due to valvular heart disease.

Diagnosis: 

Given the complex multisystem presentation, the child was admitted to the PICU for intensive monitoring and comprehensive management of this multisystem pathology. The working diagnosis is rheumatic fever.

The episode is organized into three parts:

• Pathophysiology of Acute Rheumatic Fever
• Approach to Diagnosis and Investigations
• Management and Prevention

Pathophysiology of Acute Rheumatic Fever: 

Acute rheumatic fever is an autoimmune disease initiated by a response to group A strep infection, primarily due to molecular mimicry. The streptococcal M protein has structural similarities with host proteins, leading to organ damage, especially in the heart.

Epidemiology: 

Acute rheumatic fever is most prevalent in low to middle-income areas, affecting over 80% of cases. It mainly affects children between 5 to 14 years of age, and overcrowded households and limited healthcare access increase the risk. Globally, rheumatic heart disease affects millions of people annually and claims many lives.

Jones Criteria for Diagnosis: 

The Jones criteria help diagnose acute rheumatic fever. For a definitive diagnosis, evidence of a preceding group A strep infection is required. Major manifestations include carditis, arthritis, erythema marginatum, subcutaneous nodules, and Sydenham's chorea. Minor criteria include fever, elevated inflammatory markers, prolonged PR interval on EKG, and mild joint issues.

Differentiating Low and High-Risk Populations: 

The criteria differentiate between low and high-risk populations based on the epidemiology of acute rheumatic fever. The presentation of arthritis varies, and the thresholds for fever or inflammatory marker elevation are lower in high-risk populations.

Diagnostic Approach:

Diagnosis includes throat swab, anti-streptolysin O antibody titers, anti-DNAse B titers, CBC with differential, blood cultures, inflammatory markers, EKG, chest X-ray, and echocardiography. Joint analysis may be performed if needed.

Sydenham's Chorea:

Sydenham's chorea is marked by involuntary movements, primarily in the trunk and limbs, and it often resolves within 12 to 15 weeks with treatment.

Management of Acute Rheumatic Fever: 

Management includes eradicating the remaining strep infection, controlling inflammation, and preventing recurrence. Penicillin or amoxicillin is used to treat the infection, while aspirin or NSAIDs are used to manage inflammation. In severe cases, systemic steroids may be considered. Cardiac surgery should be delayed until acute inflammation resolves. Prophylactic antibiotics are used for prevention.

Conclusion: 

Rheumatic fever management requires a holistic approach, encompassing infection control, inflammation management, and long-term prevention. Early recognition, thorough diagnostics, and prophylactic antibiotics play essential roles in managing this condition.

Future Directions: 

Research is needed for early detection using biomarkers and the development of a group A strep vaccine.

Closing Remarks: 

As pediatric intensivists, we play a pivotal role in primary prevention by advocating for awareness and prompt treatment of group A strep infections.

Thank you for listening to PICU Doc on Call. Please subscribe, share your feedback, and visit our website at picudoconcall.org for more information. Stay tuned for our next episode.

Introduction: 

Welcome to "PQ Doc On Call," a podcast dedicated to current and aspiring intensivists. Hosted by Dr. Pradeep Kamar from Children's Healthcare of Atlanta, Emory University School of Medicine, and Dr. Rahul Damia from Cleveland Clinic Children's Hospital, both passionate PICU physicians.

You will hear:

This episode dives into the management of pediatric drowning cases in the PICU, providing valuable insights into assessment, pathophysiology, and practical management strategies.

Case Presentation: 

An 18-month-old girl was admitted to the PICU following a submersion incident in a residential pool. The child's initial unresponsiveness and subsequent clinical deterioration presented challenges for the PICU team, including respiratory distress, electrolyte imbalances, and potential neurological complications.

Key Elements from the Case:

• Severe acute respiratory failure following submersion
• Abnormal electrolytes (hyponatremia)
• Neurological insult requiring ongoing monitoring

Definitions and Terminology:

Clarification of drowning terminology, emphasizing uniform definitions and avoiding outdated terms like "near drowning." Key terms include primary vs. secondary drowning, saltwater vs. freshwater, intentional vs. non-intentional, and fatal vs. non-fatal drowning incidents.

Pathophysiology:

• Airway Reflexes: Initial reflex laryngospasm triggered by liquid penetration, followed by relaxation due to hypoxia, hypercarbia, and acidosis.
• Gas Exchange Compromise: Decreased functional residual capacity leading to impaired oxygen uptake and CO2 elimination.
• Pulmonary Complications: Pulmonary edema, surfactant washout, increased pulmonary vascular resistance, and shunting, impacting oxygen delivery.

Management Strategies:

• Out-of-Hospital: Aggressive on-site CPR and advanced life support are crucial for favorable outcomes. Swift control of hypoxia and acidosis is vital.
• In-PICU: Ventilation strategies resembling ARDS management (low tidal volume, low plateau pressures, high PEEP). Consider neurological exam, continuous EEG, and neuromuscular blockade if needed.
• Prognostic Factors: Duration of submersion, time to effective CPR, initial GCS, apnea persistence, pH levels, and neurologic status.

Prevention:

Empowering prevention through measures like fencing around pools, teaching children to swim, and vigilant adult supervision can significantly reduce the risk of pediatric drowning incidents.

Conclusion:

"PQ Doc On Call" underscores the importance of timely, effective CPR, swift management of hypoxia and acidosis, and vigilant neurological assessment in pediatric drowning cases. Prevention remains paramount in avoiding such incidents.

Stay tuned for more engaging episodes from PICU Doc On Call! Don't forget to subscribe, share your feedback, and review the podcast on your preferred platform. For more information and resources, visit picudoconcall.org.

In this episode of PICU Doc On Call, your hosts Pradip Kamat and Rahul Damania, experienced Pediatric ICU physicians, take you on an enlightening journey through the intricate landscape of lactic acidosis. Join us as we unravel the complexities, share clinical insights, and provide practical guidance on diagnosing and managing this critical condition in the acute care pediatric setting.

You will hear:

Case Presentation:

4-year-old boy with hypotension, fatigue, rash, and respiratory distress

Recent COVID-19 exposure, concerning respiratory symptoms

Hypotensive, tachycardic, tachypneic, low pulse oximetry reading

Swollen red lips, erythematous rash, hepatomegaly

High-flow nasal cannula, resuscitation, epinephrine infusion

Initial arterial blood gas: pH 7.22, lactate 4.5 mMol/L

Definition of Lactic Acidosis:

• Hyperlactatemia and lactic acidosis criteria
• Causes: impaired tissue oxygenation or mitochondrial dysfunction

Types of Lactic Acidosis:

• Type A: Impaired O2 delivery, shock-related
• Type B: Impaired O2 utilization, toxins, infections

Lactate Measurement:

• Comparability between POCT and central lab analysis
• Role of lactate measurement in pediatric sepsis

Lactic Washout:

• Rising lactate with re-established oxygen delivery
• Impaired clearance in microcirculation, liver, kidney
• Monitoring trends with clinical exams and lab surrogates

Bicarbonate Therapy:

• Role in Type A lactic acidosis
• Controversy, indications, and potential complications

Conclusion:

PICU Doc On Call podcast explores the intriguing case of a 4-year-old boy with lactic acidosis, highlighting the clinical intricacies of diagnosing and managing this condition. The hosts, Pradip Kamat and Rahul Damania provide insightful discussions on the different types of lactic acidosis, the physiological mechanisms behind it, and the role of bicarbonate therapy. The episode emphasizes the importance of addressing underlying causes and offers valuable clinical pearls for managing pediatric patients with lactic acidosis.

Stay tuned for more engaging episodes from PICU Doc On Call! Don't forget to subscribe, share your feedback, and review the podcast on your preferred platform. For more information and resources, visit picudoconcall.org.

In this episode of PICU Doc On Call, Dr. Pradip Kamat and Dr. Rahul Damania discuss a case of a 4-year-old girl with bite marks and swelling of her foot, presenting with concerning vital signs and abnormal labs. They explore snake envenomation and its management in the pediatric critical care setting.

Snakes with venom-delivering fangs, primarily Elapidae and Viperidae, are responsible for most human envenomations and fatalities. We're focusing on Pit Vipers today, including rattlesnakes, cottonmouths, and the copperhead. Elapids, such as the coral snake, differ by having round pupils, short fangs, and no facial pit.

Snakebite incidents can happen when toddlers unintentionally disturb snakes, particularly in low-light conditions or grassy areas. Teenagers trying to capture snakes are another frequent group presenting with upper extremity bites. 

Pathophysiology of Snake Envenomation

Snake venoms contain toxic proteins that affect various physiological systems, leading to neurotoxic, hemotoxic, myotoxic, or cytotoxic effects. Envenomation can happen immediately or be delayed, presenting with various clinical and laboratory anomalies.

The impact of a snakebite depends on the snake type, fang size, and venom injection site. Effects may include cytotoxicity, lymphatic system damage, platelet dysfunction, neurotoxicity, cardiotoxicity, hypotension, and nephrotoxicity.

In snakebite cases, prehospital care involves immediate EMS call and ensuring airway, breathing, and hemodynamic stability. In the hospital, general supportive care is crucial, and antivenin administration depends on clinical presentation and snake type.

Antivenin dosage is challenging due to unknown venom load, and its choice depends on safety, kinetics, cost, and the specific snake involved. Smaller fragments of antivenin have larger distribution volumes and shorter half-lives. Recurrence, anaphylaxis, and serum sickness are potential side effects of antivenin.

• A high index of suspicion is required to diagnose snake envenomation.
• Antivenin is the mainstay of therapy, and rapid transport to a facility with antivenin is crucial.
• Patients should be educated about recurrence, serum sickness, and lifestyle adjustments after a pit viper bite.

Thank you for listening to this episode on snake envenomation in the PICU. For more episodes, visit our website picudoconcall.org. Stay tuned for our next episode! Don't forget to share your feedback and subscribe to our podcast.

In this episode PICUDoc On Call, we discuss the case of a six-month-old ex-preemie with bacterial meningitis who presents with symptoms of cerebral sinus venous thrombosis. We explore the anatomy of the venous distribution in the brain and the clinical syndromes associated with sinus venous thrombosis. Our focus is on the imaging techniques, laboratory tests, and management strategies involved in diagnosing and treating this challenging condition.

You will learn:

• A six-month-old ex-preemie presents with persistent fever, recurrent emesis, and increased somnolence.
• The patient experiences eye rolling and decreased oxygen saturation, prompting a visit to the emergency department.
• Physical examination reveals rigidity in all four limbs, and a head CT shows dilated ventricles and encephalomalacia.
• Lumbar puncture confirms an infection, and the patient is admitted to the hospital.
• After a 14-day course of antibiotics, the patient's clinical status worsens, leading to intubation and neurosurgery consultation.
• An MRI confirms cerebral venous sinus thrombosis.

Anatomy of Venous Distribution in the Brain:

• Dural venous sinuses serve as conduits for venous blood return from the brain to the internal jugular veins.
• The superior sagittal sinus, cortical veins, transverse sinus, sigmoid sinus, and internal jugular vein are key components of the venous drainage system.

Clinical Syndromes of Sinus Venous Thrombosis:

• Symptoms can be related to elevated intracranial pressure or focal brain damage from venous ischemia, infarction, or hemorrhage.
• Headache, seizures, focal neurologic deficits, and cranial nerve paralysis are common presentations.
• Cavernous sinus thrombosis can cause periorbital pain, ocular chemos, and paralysis of cranial nerves passing through the sinus.

Risk Factors for Cerebral Sinus Venous Thrombosis:

• Dehydration, CNS or sinus infections, intracranial surgery, autoimmune disorders, genetic syndromes, metabolic syndromes, medications, and genetic thrombophilic states can predispose children to thrombosis.
• Thorough evaluation for risk factors, including thrombophilia, is recommended in children with cerebral venous thrombosis.

Imaging and Laboratory Tests:

• CT and MRI with contrast-enhanced venography are preferred imaging tools to detect cerebral sinus venous thrombosis.
• Non-enhanced CT scans and T1/T2-weighted MRI scans show characteristic signs of thrombosis.
• Lab tests include CBC with differential, DIC panel, comprehensive metabolic panel, ESR, and specific thrombophilia tests.

Management Strategies:

• Supportive care, including airway management, hemodynamics, and neurologic monitoring, is crucial.
• Consultation with a multidisciplinary team (neurosurgeons, neuro-interventional radiologists, hematologists, etc.) is necessary.
• Anticoagulation therapy with heparin is initiated and closely monitored.
• Surgical interventions (e.g., EVD placement, ventricular peritoneal shunt, decompressive hemicraniectomy) may be required in severe cases.
• Long-term rehabilitation may be necessary for neurological deficits.

In summary:

Cerebral sinus venous thrombosis in pediatric patients requires a multidisciplinary approach for prompt diagnosis and management. Recognizing the clinical signs, conducting appropriate imaging and laboratory tests, and initiating timely interventions are crucial for improved outcomes.